PD is neuropathologically characterised by alpha-synuclein inclusions in neuronal cell bodies (Lewy bodies). Although it is primarily a movement disorder, almost half of the patients also develop dementia within 10 years from diagnosis. Cortical LB pathology and tau tangles are thought to underlie PD dementia, but other mechanisms may contribute.
We hypothesize that inflammatory change begins early in the disease and spreads throughout the brain as a ‘leading front’ in advance of Lewy body and neurofibrillary tangle formation. This inflammation, which occurs in response to pathological extracellular oligomeric proteins and early cell damage, catalyses the neurodegenerative process and is a better correlate of clinical outcome than either the Lewy body or Alzheimer-type pathology. This has important implications for disease-modifying therapies for this devastating complication of PD.
Cross-sectional and cohort studies
Magnetic resonance imaging (MRI)
Positron Emission Tomography (PET)
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Associated News Items
Scott KM, Kouli A, Yeoh SL, Clatworthy MR and Williams-Gray CH (2018), “A Systematic Review and Meta-Analysis of Alpha Synuclein Auto-Antibodies in Parkinson's Disease ” Front Neurol 9:815.
Bhosale G, Sharpe JA, Koh A, Kouli A, Szabadkai G, Duchen MR. (2017), “Pathological consequences of MICU1 mutations on mitochondrial calcium signalling and bioenergetics.” Biochim Biophys Acta Mol Cell Res. Volume 1864, Issue 6